Neurogenesis redirects β-catenin from adherens junctions to the nucleus to promote axonal growth

Here, we show that, in the developing spinal cord, after the early Wnt-mediated Tcf transcription activation that confers dorsal identity to neural stem cells, neurogenesis redirects beta-catenin from the adherens junctions to the nucleus to stimulate Tcfoependent transcription in a Wnt-independent manner. This new beta-catenin activity regulates genes implicated in several aspects of contralateral axon growth, including axon guidance and adhesion. Using liv e imaging of ex-vivo chick neural tube, we showed that the nuclear accumulation of beta-catenin and the rise in Tcfoependent transcription both initiate before the dismantling of the adherens junctions and remain during the axon elongation process. Notably, we demonstrated that beta-catenin activity in post-mitotic cells depends on TCF7L2 and is central to spinal commissural axon growth. Together, our results reveal Wnt-independent Tcf/beta-catenin regulation of genes that control the growth and guidance of commissural axons in chick spinal cord.

Automated summary

In the developing spinal cord, neurogenesis stimulates Tcf-dependent transcription through the nuclear accumulation of beta-catenin, independently of Wnt signaling. This process regulates genes involved in contralateral axon growth, including axon guidance and adhesion. These findings demonstrate the importance of Wnt-independent Tcf/beta-catenin regulation in controlling commissural axon growth in the chick spinal cord.